Oh happy day. A family of mysterious microscopic parasites infesting mainly fish, but that could possibly infect everything from frogs to Harvard grads, turn out to be degenerate jellyfish.
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The genetic analysis of these animals, known as myxozoans, astonished the zoologists at Tel Aviv University to such a degree that they suggest the whole concept of what an "animal" is might need reweighting.
Why? Because it is, we now know, a jellyfish but has lost its jellyfish characteristics to a degree that hadn't been thought likely or even possible.
It would be like finding a one-celled creature and discovering that genetically, it's a mammal that had lost its genes for lactation and keratinaceous hair, explains team leader Dorothee Huchon of the Department of Zoology Tel Aviv University, who worked on the beasts with scientists from the U.S., and France.
Not clear? It's like finding an amoeba-like parasite that infects goats and discovering that it is really first cousin to a cat, but had lost most of its feline genes, from the ones governing the meow to the genes needed for intercellular communication within the body.
Also, the jellyfish we know and love generally aren't parasitic. One exception is the Polypodium hydriforme, but unlike myxozoans, does not have a degenerate body form, the scientists point out. It has perfectly "conventional cnidarian-like features, including tentacles, a gut, and a mouth."
Our myxozoans have none of that. They degenerated, through extremely rapid evolution, into single cells (!) or animals consisting of a few cells, that no longer live on their own, but as parasites. What genome they have left is among the smallest discovered in the animal kingdom, says Huchon, co-author of the paper "Genomic insights into the evolutionary origin of Myxozoa within Cnidaria" published in PNAS.
"The Myxozoa represent an extreme example of degeneration of body plans due to parasitism," writes the scientific team, whose work was supported chiefly by a BSF-NSF grant, which backs Israeli-American collaboration in science.
"Their DNA is completely crazy," chuckles Huchon. "Every time we check a gene, we find it very different from similar genes. it had to have undergone very rapid evolution, much faster than ours." (Or course, they do have rather shorter life spans, so that makes sense.)
In short, though suspecting they were cnidaria, nobody thought these miniscule parasitic pests could possibly be jellyfish that had lost most of their jellyfish genes, but they are.
It's a girl, it's a boy, it's a medusa
There had been thought to be some 10,000 species of cnidarians, a family that includes coral, jellyfish, sea anemones - and now, following genetic analysis by an Israeli-American team headed by Huchon, myxozoans have joined the list. Which means there are some 12,000 species of cnidarians; or, myxozoans seem to represent about 20% of cnidarian diversity, which is huge, Huchon points out.
For all their structural and genetic simplicity, myxozoans reproduce sexually, not that we know where, and have a complex life cycle. Almost all of the 2,000-plus myxozoan species need both worms and fish to complete the cycle.
Which worms, by the way? Who cares – "We know about myxozoans in fish because we eat fish," points out Huchon. "However, since no one really cares about diseases in tiny worms, we do not know the complete life cycle of most myxozoan species."
The various myxozoans infect different fish in different ways, says Huchon. One might infect the nervous system, another the gut, a different type might infect muscle and yet another, the gall bladder.
In any case, they are a plague to fish farms, though Huchon qualifies that one fish generally can't infect another. That isn't how myxozoans roll. The worm is necessary for the life cycle. But if worm and fish and myxozoans are there, it's all over. (There are also some few myxozoans that don't need the worm phase.)
Even worse for fish farmers: they may not be able to sell infected fish. For instance, one type of this creature that infects salmon targets the muscle tissue, creating cysts. Living fish do not show symptoms of infection, but once dead, the cysts induce myoliquefaction, rendering the fish fillets bad to eat, explains Huchon. This causes a huge loss to the salmon industry.
With hindsight, the loss of genes as the animals receded into single-cellhood makes sense. The scientists discovered depletion of expressed genes in categories related to body development, cell differentiation (which means genes responsible for turning one cell into a brain cell and one into a kidney cell, and so on), and cell–cell communication, they explained.
If your whole body is one cell, you don't need genes that govern communication with other cells.
For what it's worth, the usual myxozoan cell features on its outside what zoologists call a "polar capsule," which are something like sucker feet on octopus tentacles. They probably stick the little animal to its unhappy host. These suckers bear remarkable similarity to the stinging structures (nematocysts) of corals, sea anemones, and the like, which suggests they evolved from these animals' nematocysts. The genetic analysis supports that theory.
So, do we have parasitic jellyfish somewhere in our bodies, like rather too many of us discovered we host toxoplasmosis parasites in our brains?
Probably not, says Huchon. Insofar as is known know, this is mainly a fish (and worm) problem, though it has been found - very rarely - in frogs, ducks and shrews, most likely ones living near water. People with compromised immune systems might be more at risk and, she adds, myxozoans have been isolated from the stools of people who ate fish carrying the parasite. But were the people themselves infected? We don't think so.